Effect of potassium on distal nephron hydrogen ion secretion in the dog.
The purpose of these investigations was to determine whether potassium might influence the DNHS and, if so, to gain insight into the mechanisms involved. Since DNHS is decreased by ECF volume expansion, dogs were studied in both normovolemic and ECF volume-expanded states. DNHS was assessed in vivo by examining the U-B PCO2. In dogs with an expanded ECF volume, the U-B PCO2 at comparable urine bicarbonate concentrations was almost 50% lower than in the normovolemic dogs. Despite hyperkalemia and kaluresis, the U-B PCO2 was minimally affected by potassium infusion in the dogs with an expanded ECF volume. In contrast, in the normovolemic dogs, the U-B PCO2 was much higher before potassium administration and it decreased after potassium infusion to levels comparable to those observed in the dogs with ECF volume expansion. The U-B PCO2 in the normovolemic dogs was inversely related to the rate of potassium excretion when this rate was less than 150 muEq/min. Amiloride, an agent that decreases the electrical gradient favoring DNHS, caused only a small fall in the U-B PCO2 in potassium-loaded dogs with either a normal or an expanded ECF volume. Although other explanations are possible, we favor the hypothesis that the secretion of potassium into the distal nephron led to a reduced rate of hydrogen ion secretion provided that there was a significant avidity for sodium reabsorption.
D000042:Absorption; D000818:Animals; D001639:Bicarbonates / Q000652:urine; D002245:Carbon Dioxide / Q000032:analysis; D004285:Dogs; D005110:Extracellular Space; D006863:Hydrogen-Ion Concentration; D007684:Kidney Tubules / Q000378:metabolism*; D007686:Kidney Tubules, Distal / Q000378:metabolism*; D010313:Partial Pressure; D011188:Potassium / Q000494:pharmacology*; D012964:Sodium / Q000378:metabolism
D001639:Bicarbonates; D002245:Carbon Dioxide; D012964:Sodium; D011188:Potassium